TBI Treatment Guide PDF

TRAUMATIC BRAIN INJURY Traumatic Brain Injury (TBI) Alteration in brain function or evidence of brain pathology caused by an external force EXTRA-AXIAL HEMMORHAGE EDH: epidural hematoma SDH: subdural hematoma SAH: subarachnoid hemorrhage INTRA-AXIAL HEMMORHAGE DAI: diffuse axonal injury IVH: intrave...

TRAUMATIC BRAIN INJURY Traumatic Brain Injury (TBI) Alteration in brain function or evidence of brain pathology caused by an external force EXTRA-AXIAL HEMMORHAGE EDH: epidural hematoma SDH: subdural hematoma SAH: subarachnoid hemorrhage INTRA-AXIAL HEMMORHAGE DAI: diffuse axonal injury IVH: intraventricular hemorrhage ICH: intracerebral hemorrhage TBI Primary injury Secondary injury PREDICTORS OF POOR OUTCOMES Elevated ICP Herniation Absent cough and gag reflexes Low GCS scores Over breathing the ventilator HYPEROSMOLAR THERAPY CEREBRAL EDEMA Causes Disruption of blood brain barrier Local inflammation Vascular changes Altered cellular metabolism Contributes to elevated ICP Poor neurologic outcomes Mortality GOALS OF ICP MANAGEMENT Maintain cerebral perfusion pressure (CPP) Provide adequate blood flow to brain CPP = MAP – ICP Goal CPP: 60-70 mmHg MAP = !"#$%('"#) ) Goal ICP: < 22 mmHg HYPEROSMOLAR THERAPY Osmotic gradient Decrease blood viscosity Increased microcirculatory flow MANNITOL Osmotic diuretic Adverse effects Hypernatremia Hypovolemia Renal dysfunction HYPERTONIC SALINE Advantages: increases MAP and decreases ICP = improved CPP Monitoring: serum sodium levels, renal function Adverse effects: hypernatremia HYPEROSMOLAR THERAPY Hypertonic Saline Mannitol ICP reduction onset < 5 min 15 - 30 min ICP reduction duration Up to 12 hrs 1.5 to 6 hrs Rebound effect None Possible Diuretic effect None Yes ~ ↓MAP EARLY SEIZURE PROPHYLAXIS SEIZURE PROPHYLAXIS Recommended to prevent early posttraumatic seizures within 7 days of injury RISK FACTORS OF EARLY PTS GCS < 10 Immediate seizures Subdural, epidural, or intracerebral hematoma Post-traumatic amnesia lasting longer than 30 mins Cortical contusion Linear or depressed skull fracture Age < 65 years Penetrating head injury Chronic alcoholism ANTIEPILEPTIC THERAPY Phenytoin Most data to support its use Not used as often Levetiracetam Used more commonly PHENYTOIN Monitoring Dose titrated based on phenytoin levels Not as well tolerated as levetiracetam More sedating LEVETIRACETAM Shown to be as effective as phenytoin in preventing seizures Benefits Improved safety profile Easy administration Few DDI Safe in pregnancy No drug monitoring required 1:1 IV to PO conversion DURATION OF THERAPY 7 days post TBI VTE PROPHYLAXIS BACKGROUND High risk for VTE Hypercoagulable state from: Primary brain injury Periods of prolonged immobilization Focal motor deficits Predictors of DVT Age SAH ISS > 15 Extremity injury AGENTS Compression devices (SCDs), graduated compression stockings LMWH or low-dose UFH TIMING LMWH or UFH within 24-48 hr from stable head CT OTHER AGENTS PROPOFOL Sedative of choice in TBI patients Decreases ICP Rapid onset, short duration Possible neuroprotective effects No mortality benefit No effects on neurological improvement Monitoring Triglyceride levels Propofol related infusion syndrome (PRIS) PENTOBARBITAL NOT a 1st line agent Elevated ICP refractory to other agents Barbiturate coma Concerns Long half-life Hypotension METHYLPREDNISOLONE CRASH (2004) Increased mortality AVOID steroid use in TBI AMANTADINE Improved recovery time in severe TBI Not in the acute phase No effect on ICP Benefits stop with discontinuation of therapy